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Tetsuya Toyono, Shotaro Asano, Takashi Miyai, Kodai Kitamoto, Suguru Nakagawa, Masahiko Kuroda, Albert Jun, Tomohiko Usui; MicroRNA-184 overexpression suppresses TGFβ/Smad signal in human corneal endothelial cells. Invest. Ophthalmol. Vis. Sci. 2018;59(9):1368.
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It has been reported that microRNA (miR)-184 is decreased in corneal endothelial cells of Fuchs endothelial corneal dystrophy (FECD). The previous study indicated that TGFβ/Smad signal induces apoptosis via endoplasmic reticulum stress in FECD. In the current study, we transfected miR-184 mimics into human corneal endothelial cells derived from FECD patient, and evaluated the expression levels of molecules related to TGFβ/Smad signaling.
An immortalized corneal endothelial cell line (iFECD) from FECD patient was used in this study. Single strand miR-184 mimics (miR-184 psh) or scrambled single strand RNA (scramble psh) was transfected into iFECD. Quantitative reverse transcriptase–polymerase chain reaction (qRT-PCR) was conducted to compare the mRNA expressions of TGFβ receptor 2 (TGFBR2), Smad2 and Smad3. The protein levels of TGFBR2, TGFB2, Smad2, Smad3 and phosphorylated Smad2/3 were evaluated by western blotting.
TGFBR2 mRNA expression by qRT-PCR was significantly decreased in cells transfected with miR-184 psh compared with those transfected with scramble psh (p = 0.029). Western blotting showed phosphorylation of Smad2/3 was significantly decreased in cells transfected with miR-184 psh compared with those transfected with scramble psh (p = 0.028, Wilcoxon’s rank sum test).
Overexpression of miR-184 might suppress of TGFβ/Smad signal in FECD.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.
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